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Voluntary exercise following traumatic brain injury: brain-derived neurotrophic factor upregulation and recovery of function.
Neuroscience. 2004; 125(1):129-39.N

Abstract

Voluntary exercise leads to an upregulation of brain-derived neurotrophic factor (BDNF) and associated proteins involved in synaptic function. Activity-induced enhancement of neuroplasticity may be considered for the treatment of traumatic brain injury (TBI). Given that during the first postinjury week the brain is undergoing dynamic restorative processes and energetic changes that may influence the outcome of exercise, we evaluated the effects of acute and delayed exercise following experimental TBI. Male Sprague-Dawley rats underwent either sham or lateral fluid-percussion injury (FPI) and were housed with or without access to a running wheel (RW) from postinjury days 0-6 (acute) or 14-20 (delayed). FPI alone resulted in significantly elevated levels of hippocampal phosphorylated synapsin I and phosphorylated cyclic AMP response element-binding-protein (CREB) at postinjury day 7, of which phosphorylated CREB remained elevated at postinjury day 21. Sham and delayed FPI-RW rats showed increased levels of BDNF, following exercise. Exercise also increased phosphorylated synapsin I and CREB in sham rats. In contrast to shams, the acutely exercised FPI rats failed to show activity-dependent BDNF upregulation and had significant decreases of phosphorylated synapsin I and total CREB. Additional rats were cognitively assessed (learning acquisition and memory) by utilizing the Morris water maze after acute or delayed RW exposure. Shams and delayed FPI-RW animals benefited from exercise, as indicated by a significant decrease in the number of trials to criterion (ability to locate the platform in 7 s or less for four consecutive trials), compared with the delayed FPI-sedentary rats. In contrast, cognitive performance in the acute FPI-RW rats was significantly impaired compared with all the other groups. These results suggest that voluntary exercise can endogenously upregulate BDNF and enhance recovery when it is delayed after TBI. However, when exercise is administered to soon after TBI, the molecular response to exercise is disrupted and recovery may be delayed.

Authors+Show Affiliations

David Geffen School of Medicine at UCLA, Division of Neurosurgery, Los Angeles, CA 90095-7039, USA. ggriesbach@mednet.ucla.eduNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
Journal Article

Language

eng

PubMed ID

15051152

Citation

Griesbach, G S., et al. "Voluntary Exercise Following Traumatic Brain Injury: Brain-derived Neurotrophic Factor Upregulation and Recovery of Function." Neuroscience, vol. 125, no. 1, 2004, pp. 129-39.
Griesbach GS, Hovda DA, Molteni R, et al. Voluntary exercise following traumatic brain injury: brain-derived neurotrophic factor upregulation and recovery of function. Neuroscience. 2004;125(1):129-39.
Griesbach, G. S., Hovda, D. A., Molteni, R., Wu, A., & Gomez-Pinilla, F. (2004). Voluntary exercise following traumatic brain injury: brain-derived neurotrophic factor upregulation and recovery of function. Neuroscience, 125(1), 129-39.
Griesbach GS, et al. Voluntary Exercise Following Traumatic Brain Injury: Brain-derived Neurotrophic Factor Upregulation and Recovery of Function. Neuroscience. 2004;125(1):129-39. PubMed PMID: 15051152.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Voluntary exercise following traumatic brain injury: brain-derived neurotrophic factor upregulation and recovery of function. AU - Griesbach,G S, AU - Hovda,D A, AU - Molteni,R, AU - Wu,A, AU - Gomez-Pinilla,F, PY - 2004/01/25/accepted PY - 2004/3/31/pubmed PY - 2004/6/4/medline PY - 2004/3/31/entrez SP - 129 EP - 39 JF - Neuroscience JO - Neuroscience VL - 125 IS - 1 N2 - Voluntary exercise leads to an upregulation of brain-derived neurotrophic factor (BDNF) and associated proteins involved in synaptic function. Activity-induced enhancement of neuroplasticity may be considered for the treatment of traumatic brain injury (TBI). Given that during the first postinjury week the brain is undergoing dynamic restorative processes and energetic changes that may influence the outcome of exercise, we evaluated the effects of acute and delayed exercise following experimental TBI. Male Sprague-Dawley rats underwent either sham or lateral fluid-percussion injury (FPI) and were housed with or without access to a running wheel (RW) from postinjury days 0-6 (acute) or 14-20 (delayed). FPI alone resulted in significantly elevated levels of hippocampal phosphorylated synapsin I and phosphorylated cyclic AMP response element-binding-protein (CREB) at postinjury day 7, of which phosphorylated CREB remained elevated at postinjury day 21. Sham and delayed FPI-RW rats showed increased levels of BDNF, following exercise. Exercise also increased phosphorylated synapsin I and CREB in sham rats. In contrast to shams, the acutely exercised FPI rats failed to show activity-dependent BDNF upregulation and had significant decreases of phosphorylated synapsin I and total CREB. Additional rats were cognitively assessed (learning acquisition and memory) by utilizing the Morris water maze after acute or delayed RW exposure. Shams and delayed FPI-RW animals benefited from exercise, as indicated by a significant decrease in the number of trials to criterion (ability to locate the platform in 7 s or less for four consecutive trials), compared with the delayed FPI-sedentary rats. In contrast, cognitive performance in the acute FPI-RW rats was significantly impaired compared with all the other groups. These results suggest that voluntary exercise can endogenously upregulate BDNF and enhance recovery when it is delayed after TBI. However, when exercise is administered to soon after TBI, the molecular response to exercise is disrupted and recovery may be delayed. SN - 0306-4522 UR - https://www.unboundmedicine.com/medline/citation/15051152/Voluntary_exercise_following_traumatic_brain_injury:_brain_derived_neurotrophic_factor_upregulation_and_recovery_of_function_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0306452204000764 DB - PRIME DP - Unbound Medicine ER -